AI Article Synopsis

  • - The pro-B cell stage is crucial for commitment to the B cell lineage, and the transcription factor YY1 plays a key role in this process; knocking out YY1 during this stage prevents cells from committing to B cells.
  • - Instead of developing into B cells, YY1 knockout pro-B cells can differentiate into T lineage cells in specific experimental conditions, demonstrating their ability to switch lineages.
  • - Single-cell RNA sequencing reveals that these YY1 knockout pro-B cells display a variety of transcript profiles, indicating a significant level of lineage plasticity and suggesting that YY1 is important for lineage commitment across different cell types.

Article Abstract

During B cell development, cells progress through multiple developmental stages with the pro-B cell stage defining commitment to the B cell lineage. YY1 is a ubiquitous transcription factor that is capable of both activation and repression functions. We find here that knockout of YY1 at the pro-B cell stage eliminates B lineage commitment. YY1 knockout pro-B cells can generate T lineage cells using the OP9- DL4 feeder system, as well as after injection into sub-lethally irradiated Rag1 mice. These T lineage-like cells lose their B lineage transcript profile and gain a T cell lineage profile. Single cell-RNA-seq experiments showed that as YY1 knockout pro-B cells transition into T lineage cells, various cell clusters adopt transcript profiles representing a multiplicity of hematopoietic lineages indicating unusual lineage plasticity. Given the ubiquitous nature of YY1 and its dual activation and repression functions, YY1 likely regulates commitment in multiple cell lineages.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10996465PMC
http://dx.doi.org/10.1101/2024.03.22.586298DOI Listing

Publication Analysis

Top Keywords

yy1 knockout
12
knockout pro-b
12
pro-b cells
12
unusual lineage
8
lineage plasticity
8
cells cell
8
pro-b cell
8
cell stage
8
cell lineage
8
activation repression
8

Similar Publications

Blocking adipocyte YY1 decouples thermogenesis from beneficial metabolism by promoting spermidine production.

Diabetes

December 2024

Department of Endocrinology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou 225300, China.

The accumulation of mitochondria in thermogenic adipose tissue (i.e., brown and beige fat) increases energy expenditure, which can aid in alleviating obesity and metabolic disorders.

View Article and Find Full Text PDF

Loss of DNA Polymerase β Delays Atherosclerosis in Mice Due to Inhibition of Vascular Smooth Muscle Cell Migration.

Int J Mol Sci

November 2024

Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Sciences, Nanjing Normal University, 1 Wenyuan Road, Nanjing 210023, China.

Atherosclerosis (AS) is an inflammatory disease characterized by arterial inflammation. One important trigger for AS development is the excessive migration of vascular smooth muscle cells (VSMCs); however, the mechanism underlying this phenomenon remains unclear. Therefore, we investigated the role of DNA polymerase β (Pol β), a crucial enzyme involved in base excision repair, VSMC migration, and subsequent AS development.

View Article and Find Full Text PDF
Article Synopsis
  • During B-cell development, the pro-B-cell stage is crucial for committing to the B-cell lineage, and the transcription factor YY1 plays a key role in this process.
  • Knocking out YY1 at the pro-B-cell stage stops B-cell development and enables these cells to convert into T lineage cells, demonstrating a shift in their genetic expression profiles.
  • Research involving various sequencing techniques shows that the loss of YY1 not only affects B lineage commitment but also allows pro-B cells to exhibit flexibility in developing into multiple hematopoietic lineages due to changes in chromatin accessibility.
View Article and Find Full Text PDF

Epstein-Barr Virus (EBV) is associated with numerous cancers including B cell lymphomas. In vitro, EBV transforms primary B cells into immortalized Lymphoblastoid Cell Lines (LCLs) which serves as a model to study the role of viral proteins in EBV malignancies. EBV induced cellular transformation is driven by viral proteins including EBV-Nuclear Antigens (EBNAs).

View Article and Find Full Text PDF

Neopterin mediates sleep deprivation-induced microglial activation resulting in neuronal damage by affecting YY1/HDAC1/TOP1/IL-6 signaling.

J Adv Res

July 2024

School of Life Sciences, Lanzhou University, 730030 Lanzhou, China; The First Affiliated Hospital of Medical College, Zhejiang University, Zhejiang 310000, China. Electronic address:

Article Synopsis
  • Sleep deprivation (SD) leads to hippocampal microglia activation and inflammation, which can impair learning and memory; however, the exact mechanisms behind this damage are not fully understood.
  • In this study, researchers hypothesized that Topoisomerase 1 (TOP1) could play a role in SD-induced microglial activation and neuronal damage, based on the observed increase in TOP1 levels in the hippocampus of SD mice.
  • Experiments using TOP1 knockout mice demonstrated that reducing TOP1 in microglia lessened inflammatory responses and neuronal damage, suggesting TOP1 mediates the release of harmful inflammatory factors like IL-6 during sleep deprivation.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!